Avoiding Unintended Toxicity

摘要

Amyloid-β protein (Aβ) deposition in the brain is one of the pathological hallmarks of Alzheimer's disease. Considerable data support the concept that the aggregation and accumulation of Aβ in the brain trigger a complex pathological cascade that ultimately results in neuronal dysfunction and neurodegeneration (1). Thus, therapies for Alzheimer's disease have focused mainly on preventing or slowing Aβ aggregation, neutralizing toxic Aβ aggregates, or clearing and breaking up these aggregates (2). On page 639 of this issue, Serneels et al.